The proposed studies in this grant are designed to determine mechanisms by which pharmacologic doses of prostaglandin E1 (PGE1) prevent immune complex deposition in experimental murine glomerulonephritis. Previous immunopathologic data in the NZB/W hybrid indicate that PGE1 prolongs survival by decreasing the deposition of immune complexes in glomeruli. Accompanying this is a selective suppression of antibody responses to a viral antigen (gp 70) and prevention of age-related lymphoid changes. Therapy is effective in another murine model to SLE, the MRL/1, but does not alter the course of disease in the BXSB strain. Planned investigations will extend these initial observations. Experiments will focus on drug induced changes in renal pathology, concentrations of circulating total and viral immune complexes, and alterations in peripheral lymphocyte numbers in all strains. By comparing the activities of PGE1 in these three mouse models it should be possible to determine the immunopathologic mechanisms important in these disease processes. Further studies are designed to define 1) the activity of PGE1 in antibody production and 2) the direct effects of this agent within the glomerulus.